Propofol-mediated impairment of CA1 long-term potentiation in mouse hippocampal slices

Takamatsu, Isao; Sekiguchi, Masayuki; Wada, Keiji; Sato, Tetsuo; Ozaki, Makoto

doi:10.1016/j.neulet.2005.07.043

Cited by 37 publications

(24 citation statements)

References 22 publications

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“…An inhibition of hippocampal LTP by volatile anesthetics, 6,27,28 propofol, 29 and etomidate 9 has been reported. Dependent on the mechanisms of action, isoflurane, 6 sevoflurane, 7 and etomidate 9 reduce LTP, at least partly, because of their potentiating effect on the GABAergic system.…”

Section: Discussionmentioning

confidence: 99%

Xenon Attenuates Hippocampal Long-term Potentiation by Diminishing Synaptic and Extrasynaptic N -methyl-D-aspartate Receptor Currents

Kratzer

Mattusch²,

Kochs³

et al. 2012

Anesthesiology

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Background:The memory-blocking properties of general anesthetics are of high clinical relevance and scientific interest. The inhalational anesthetic xenon antagonizes N-methyl-D-aspartate (NMDA) receptors. It is unknown if xenon affects long-term potentiation (LTP), a cellular correlate for memory formation. In hippocampal brain slices, the authors investigated in area CA1 whether xenon affects LTP, NMDA receptor-mediated neurotransmission, and intracellular calcium concentrations. Methods: In sagittal murine hippocampal brain slices, the authors investigated the effects of xenon on LTP by recording excitatory postsynaptic field potentials. Using fluorometric calcium imaging, the authors tested the influence of xenon on calcium influx during high-frequency stimulation. In addition, using the patch-clamp technique, the xenon effect on synaptic and extrasynaptic NMDA receptors and L-type calcium channels was examined. Results: In the absence of xenon, high-frequency stimulation reliably induced LTP and potentiated field potential slopes to (mean Ϯ SEM) 127.2 Ϯ 5.8% (P Ͻ 0.001). In the presence of xenon, high-frequency stimulation induced only a short-term potentiation, and field potentials returned to baseline level after 15-20 min (105.9 Ϯ 2.9%; P ϭ 0.090). NMDA receptor-mediated excitatory postsynaptic currents

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Section: Discussionmentioning

confidence: 99%

Xenon Attenuates Hippocampal Long-term Potentiation by Diminishing Synaptic and Extrasynaptic N -methyl-D-aspartate Receptor Currents

Kratzer

Mattusch²,

Kochs³

et al. 2012

Anesthesiology

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“…Furthermore, phosphorylation of the GluR1 subunit of the a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor by the activated CaMKII leads to an enhanced receptor channel conductance, 33 which plays a major role in mediating the postsynaptic mechanism of LTP. Propofol 34,35 and ketamine 36 impair learning and memory on the basis of its ability to block LTP in the hippocampus in animal models. Animal studies suggest that NMDA receptor antagonism impairs the acquisition of information by disrupting LTP in the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Propofol and Ketamine-induced Anesthetic Depth-dependent Decrease of CaMKII Phosphorylation Levels in Rat Hippocampus and Cortex

Cui

Li²,

Li³

et al. 2009

Journal of Neurosurgical Anesthesiology

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Ca/calmodulin-dependent protein kinase II (CaMKII) activation through autophosphorylation at threonine 286 was involved in the modulation of neuronal excitability and neurotransmission. Both propofol and ketamine may affect the intracellular Ca levels through N-methyl-D-aspartate receptors or voltage-dependent Ca channels, but they have different mechanisms in general anesthesia. The purpose of this study was to investigate the effects of propofol and ketamine on CaMKII total protein and phosphorylation (p-CaMKII) levels in the brain of rats. We found that both propofol and ketamine could induce a decrease of p-CaMKII, not CaMKII total protein, in an anesthetic depth-dependent manner, whereas only ketamine caused a dose (50, 100, and 150 mg/kg)-dependent depression of p-CaMKII in hippocampus and frontal cortex of rats after intraperitoneal injections for 30 minutes. The significant depressions of p-CaMKII started at 5 minutes both in hippocampus and frontal cortex of rats after 100 mg/kg propofol treatment, whereas 100 mg/kg ketamine-induced significant depression of p-CaMKII initiated at 30 minutes in hippocampus and 5 minutes (no reduction observed at 15 min) in frontal cortex of rats. The maximum reduction of p-CaMKII with both drugs was at 60 minutes, and then restored to control level at 240 minutes. In addition, we confirmed the depression of p-CaMKII in hippocampus and frontal cortex of rats after 100 mg/kg of propofol or ketamine treatment for 60 minutes by using immunostaining. These results suggested that decreased p-CaMKII levels correlate with anesthetic depths achieved by propofol and ketamine, which may be related to the effects of propofol and ketamine on central nervous system function and their clinical effect.

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“…When recordings were performed from the mPFC or basolateral amygdala (BLA), coronal brain slices (300 m thick) were prepared using a Vibratome 3000 (Vibratome, St. Louis, MO) in artificial CSF [ACSF; containing the following (in mM): 125 NaCl, 4.4 KCl, 1.5 MgSO 4 , 1.0 NaH 2 PO 4 , 26 NaHCO 3 , 10 glucose, 2.5 CaCl 2 , pH 7.4, 290 -300 mOsm/l]. When recordings were performed from the CA1 field, the hippocampus was isolated from the brain and transverse slices (400 m thick) were prepared as described previously (Nakagawa et al, 1999;Takamatsu et al, 2005) using a Vibratome 3000 in a sucrose-based cutting solution [containing the following (in mM): 234 sucrose, 25 KCl, 1.25 NaH 2 PO 4 , 10 MgSO 4 , 26 NaHCO 3 , 11 glucose, 0.5 CaCl 2 ]. The slices were maintained at room temperature in ACSF continuously bubbled with 95% O 2 /5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Facilitation of Extinction Learning for Contextual Fear Memory by PEPA: A Potentiator of AMPA Receptors

Zushida¹,

Sakurai²,

Wada³

et al. 2007

J. Neurosci.

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Contextual fear memory is attenuated by the re-exposure of mice to the context without aversive stimulus. This phenomenon is called extinction. Here, we report that a potentiator of AMPA receptors, 4-[2-(phenylsulfonylamino)ethylthio]-2,6-difluorophenoxyacetamide (PEPA), potently facilitates extinction learning in mice. C57BL/6J mice were exposed to novel context and stimulated by electrical footshock. After 24 h (extinction training) and 72 h (extinction test), the mice were repeatedly exposed to the context without footshock and the duration of their freezing response was measured. The duration of freezing response in the extinction test was consistently shorter than the value in extinction training. Intraperitoneal injection of PEPA 15 min before extinction training remarkably reduced the duration of freezing responses during the extinction training and test, compared with the vehicle-injected control mice. This action of PEPA on extinction was dose-dependent and inhibited by NBQX (1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide), an AMPA receptor antagonist. PEPA had no effect on acquisition and consolidation of fear memory itself. Electrophysiological studies suggested that PEPA activates the neural network much more potently in the medial prefrontal cortex (mPFC) than in the basolateral amygdala and hippocampal CA1 field. Quantitative PCR studies suggested the pronounced expression of PEPA-preferring AMPA receptor subunits (GluR3 and GluR4) and a splice variant (flop) in the mPFC. An intra-mPFC injection of PEPA facilitated the extinction much more potently than an intra-amygdala injection of PEPA did. These results suggest that PEPA facilitates extinction learning through AMPA receptor activation mainly in the mPFC.

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Propofol-mediated impairment of CA1 long-term potentiation in mouse hippocampal slices

Cited by 37 publications

References 22 publications

Xenon Attenuates Hippocampal Long-term Potentiation by Diminishing Synaptic and Extrasynaptic N -methyl-D-aspartate Receptor Currents

Xenon Attenuates Hippocampal Long-term Potentiation by Diminishing Synaptic and Extrasynaptic N -methyl-D-aspartate Receptor Currents

Propofol and Ketamine-induced Anesthetic Depth-dependent Decrease of CaMKII Phosphorylation Levels in Rat Hippocampus and Cortex

Facilitation of Extinction Learning for Contextual Fear Memory by PEPA: A Potentiator of AMPA Receptors

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